Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011551 (depersonalization)
 1,117 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eye Closure, Eye Movements (ECEM) is a hypnotically-based approach to treatment that incorporates eye movements adapted from the Eye Movement Desensitization and Reprocessing (EMDR) protocol in conjunction with hypnosis for the treatment of depersonalization disorder. Depersonalization Disorder has been differentiated from post-traumatic stress disorders and has recently been conceptualized as a subtype of panic disorder (Baker et al., 2003; David, Phillips, Medford, & Sierra, 2004; Segui et. al., 2000). During ECEM, while remaining in a hypnotic state, clients self-generated six to seven trials of eye movements to reduce anticipatory anxiety associated with depersonalization disorder. Eye movements were also used to process triggers that elicited breath holding, often followed by episodes of depersonalization. Hypnotic suggestions were used to reverse core symptoms of depersonalization, subjectively described as "feeling unreal" (Simeon et al., 1997).
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PMID:ECEM (Eye Closure, Eye Movements): application to depersonalization disorder. 1986 96

Depersonalization disorder (DPD) is characterized by a subjective sense of detachment from one's own being and a sense of unreality. An examination of the psychobiology of depersonalization symptoms may be useful in understanding the cognitive-affective neuroscience of embodiment. DPD may be mediated by neurocircuitry and neurotransmitters involved in the integration of sensory processing and of the body schema, and in the mediation of emotional experience and the identification of feelings. For example, DPD has been found to involve autonomic blunting, deactivation of sub-cortical structures, and disturbances in molecular systems in such circuitry. An evolutionary perspective suggests that attenuation of emotional responses, mediated by deactivation of limbic structures, may sometimes be advantageous in response to inescapable stress.
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PMID:Cognitive-affective neuroscience of depersonalization. 1989 Feb 27

It is often assumed that when confronted with an emotional event, patients with DPD inhibit information processing. It is also thought that this fosters memory fragmentation. This hypothesis has not been tested in chronic depersonalization. The aim of this study was to investigate the temporal pattern of autonomic responding to emotional material in depersonalization disorder, along with concomitant deficits in subjective and objective memory formation (i.e., difficulties to form a coherent narrative consisting of an ordered sequence of events). Participants with depersonalization disorder (n=14) and healthy control participants (n=14) viewed an emotional video clip while their skin conductance (SC) levels were measured. Peritraumatic dissociation was measured before and after the clip, and memory performance was measured 35 min after viewing. Compared to controls, depersonalized participants exhibited a distinctly different temporal pattern of autonomic responding, characterized by an earlier peak and subsequent flattening of SCLs. Maximum SCLs did not differ between the two groups. Moreover, unlike the control group, depersonalized participants showed no SC recovery after clip offset. In terms of memory performance, patients exhibited objective memory fragmentation, which they also reported subjectively. However, they did not differ from controls in free recall performance. Apparently, emotional responding in DPD is characterized by a shortened latency to peak with subsequent flattening and is accompanied by memory fragmentation in the light of otherwise unremarkable memory functioning.
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PMID:Skin conductance and memory fragmentation after exposure to an emotional film clip in depersonalization disorder. 2038 Nov 60

Depersonalization disorder is considered to be a common clinical phenomenon and disorder with an enormous gap between prevalence and detection partly due to the common interpretation of depersonalization (DP) being a negligible variant of anxiety and depression. Therefore, we sought to analyze (1) the prevalence rate of DP in a large community sample (n=5000) according to a recently developed ultra brief two-item depersonalization screener; (2) the associations with depression, anxiety, physical and mental health status; and 93) whether DP contributes independently to the health status beyond anxiety and depression. The prevalence of clinically significant DP was 0.8% (n=41), and 8.5% (n=427) endorsed at least one symptom of DP. DP was independently associated with impairment of mental and physical health status as well as with a medical history of any depressive or anxiety disorder. Despite the consistent association of DP with anxiety and depression, the shared variances were small, and DP was clearly separated from symptoms of anxiety and depression in the principal component analysis. Therefore, we conclude that the implementation of depersonalization screening might be recommended.
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PMID:Distinctiveness and overlap of depersonalization with anxiety and depression in a community sample: results from the Gutenberg Heart Study. 2112 25

The symptom of depersonalization is frequently associated with other mental disorders, physiological effects of substances or medical diseases. However, it is rare that, as in the case presented, the experiences of depersonalization form an isolated entity, a primary depersonalization disorder. Among the many psychoactive drugs studied, none of them has been shown to be the treatment of choice. Among those with which the best results are obtained are opioid receptor antagonists (naloxone and naltrexone), the combination of selective serotonin reuptake inhibitors with lamotrigine and clorimipramine. Although with virtually no evidence, we are presenting a case that responded spectacularly to methylphenidate.
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PMID:Methylphenidate in depersonalization disorder: a case report. 2127 25

Low-dose ketamine administration mimics, both clinically and on gross neuroimaging, depersonalization disorder. The perceptual effects of ketamine may be due to secondary stimulation of glutamate release and lamotrigine, possibly by inhibited glutamate release, may reduce some of ketamine's so-called dissociative effects. However, lamotrigine does not seem to be useful in the treatment of depersonalization disorder. Glutamate release in prefrontal cortex is increased by subanaesthetic doses of ketamine, resulting in increased inhibition, possibly via intercalated GABAerg cells, of projections from amygdala, affecting structures critically involved in depersonalization. I speculate that, in depersonalization disorder, the increased glutamate activity in prefrontal cortex is due to intrinsic imbalance, resulting in long-term potentiation, at the postsynaptic glutamate receptors on the GABAerg interneurons while the same receptor abnormality at the synapses on the intercalated GABAerg cells of the amygdala result in long-term depression in the case of either normal or high glutamate release.
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PMID:Depersonalization disorder may be related to glutamate receptor activation imbalance. 2174 42

A significant association between anxiety and depersonalization has been found in healthy controls and psychiatric patients irrespective of underlying conditions. Although patients with depersonalization disorder (DPD) often have a history of severe anxiety symptoms, clinical observations suggest that the relation between anxiety and depersonalization is complex and poorly understood. Using relevant rating scales, levels of anxiety and depersonalization were assessed in 291 consecutive DPD cases. 'High' and 'low' depersonalization groups, were compared according to anxiety severity. Correlation and multivariate regression analyses were also used to assessed the contribution of anxiety to the phenomenology and natural course of depersonalization. A low but significant association between depersonalization and anxiety (as measured by Beck's Anxiety Inventory) was only apparent in those patients with low intensity depersonalization, but not in those with severe depersonalization. Levels of anxiety did not seem to make specific contributions to the clinical features of depersonalization itself, although DPD patients with high anxiety seem characterised by additional non-specific perceptual symptoms. The presence of a 'statistical dissociation' between depersonalization and anxiety adds further evidence in favour of depersonalization disorder being an independent condition and suggests that its association with anxiety has been overemphasized.
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PMID:Depersonalization disorder and anxiety: a special relationship? 2241 60

The rationale, research literature, and proposed changes to the dissociative disorders and conversion disorder in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) are presented. Dissociative identity disorder will include reference to possession as well as identity fragmentation, to make the disorder more applicable to culturally diverse situations. Dissociative amnesia will include dissociative fugue as a subtype, since fugue is a rare disorder that always involves amnesia but does not always include confused wandering or loss of personality identity. Depersonalization disorder will include derealization as well, since the two often co-occur. A dissociative subtype of posttraumatic stress disorder (PTSD), defined by the presence of depersonalization or derealization in addition to other PTSD symptoms, is being recommended, based upon new epidemiological and neuroimaging evidence linking it to an early life history of adversity and a combination of frontal activation and limbic inhibition. Conversion disorder (functional neurological symptom disorder) will likely remain with the somatic symptom disorders, despite considerable dissociative comorbidity.
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PMID:Dissociative disorders in DSM-5. 2339 28

Depersonalization disorder is associated with emotional responding deficits. Ability to regulate emotion was measured by heart rate, skin conductance, and subjective responses to pictures. Compared to controls, depersonalized participants were better able to suppress, but not enhance, emotions irrespective of valence (heart rate). Emotion regulation in depersonalization merits further study.
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PMID:Preliminary physiological evidence for impaired emotion regulation in depersonalization disorder. 2350 19

A high variety of factors were found to be implicated in the emergence of depersonalization episodes. The remarkable case of a patient who developed a hemi-depersonalization syndrome is reported in a patient with known obsessive-compulsive disorder. He complained of feeling his left half of the body as if it was detached from him. The part of the body that was perceived as estranged was inconsistent with the anatomical distribution of the nervous system as the entire left part of his body was concerned, from head to toe. He always remained aware that the sensations were not real, and felt like being an outside observer of the left side of his body. He also developed an isolated delusional idea. The hemi-depersonalization syndrome as well as the delusional idea did not respond to citalopram 20 mg/day, but remitted rapidly under olanzapine 10 mg/day, the obsessive-compulsive symptomatology persisting for several weeks. From the course of hemi-depersonalization syndrome and the available literature, it is concluded that this syndrome is independent from the concomitant OCD and that the observed hemi-depersonalization syndrome is likely to be a manifestation of a psychotic reaction which consisted of both the hemi-depersonalization and delusions.
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PMID:Hemi-depersonalization syndrome. 2494 42


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